[Detection of the presence of ethyl alcohol in amniotic fluid drawn by trans-abdominal echo-guided amniocentesis].
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Abdomen↗
Biomedical subjects
R Ferrario
Publications and source records attributed to R Ferrario.
Benzoylalanine analogues as inhibitors of rat brain kynureninase and kynurenine 3-hydroxylase.
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Alanine↗
Value of buserelin testing in the evaluation of hirsute women.
It has been recently reported that many hirsute women are affected with functional ovarian hyperandrogenism (FOH)-a term that encompasses the heterogeneous polycystic ovary syndrome- and show an abnormal ovarian steroidogenic response to gonadotropin-releasing hormone (Gn-RH) agonists. The aims of the present study were to determine the prevalence of FOH by the assessment of 17-hydroxyprogesterone (17-OHP) response to the Gn-RH agonist buserelin, to correlate these abnormal responses to other parameters suggestive of PCOS, and to assess the possible adrenal origin of hyperandrogenism. Therefore, in 33 consecutive women with hirsutism serum LH, FSH, 17-OHP, dehydroepiandrosterone sulfate (DHEA-S), androstenedione (A), cortisol levels were evaluated in basal conditions and after the administration of buserelin (0.5 mg sc) and ACTH (tetracosactide 0.25 mg iv). Two patients were affected with a non classic congenital adrenal hyperplasia (CAH)-21OH deficiency. In 5 other women ACTH test caused a rate increase 17-OHP (30-0)/30 min > 19 nmol/L/min (0.25 +/- 0.03; mean +/- SE), suggesting the possible existence of heterozygote non classic CAH-21OH. One patient showed a DHEA-S response to ACTH (from 10.3 to 17.2 mumol/L), which was compatible with late-onset 3 beta-Hydroxy-delta 5 steroid dehydrogenase deficiency. Out of the 25 patients with normal responsiveness to ACTH, 11 women (group A) showed higher 17-OHP and A levels, in comparison to normal women, both in basal conditions (17-OHP = 4.18 +/- 0.72 vs 1.74 +/- 0.34 nmol/L, p < 0.005; A = 11.8 +/- 1.2 vs 6.0 +/- 0.7 nmol/L, p < 0.05) and after buserelin (17-OHP = 15.61 +/- 1.31 vs 6.96 +/- 0.9 nmol/L; A = 19.0 +/- 1.9 vs 7.5 +/- 0.8 nmol/L; p < 0.001). In 6 of these 11 patients basal and buserelin-stimulated LH levels were higher than in normals. The remaining 14 patients (group B) showed normal baseline and buserelin-stimulated 17-OHP and A concentrations. In this group only 2 patients had high basal and stimulated LH levels. An augmented LH/FSH ratio was present in 5 and 1 cases of groups A and B, and polycystic ovaries at ultrasonography were observed in 7 and 8 cases of groups A and B, respectively. It is to note that an abnormal 17-OHP response to buserelin was present also in 3 of the 5 patients with abnormal 17-OHP rise after ACTH test, suggesting an adrenal and ovarian cause of hyperandrogenism. In conclusion, an abnormal response to one or both stimulation test was present in 57% of cases: an adrenal origin of hirsutism was detected in 15%, a combined adrenal and ovarian origin was found in 9% and an ovarian cause was present in 33%. Buserelin testing is an useful means to reveal the presence of FOH.
17-alpha-Hydroxyprogesterone↗
A European nursing perspective of communication.
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Communication↗
Long-term thromboxane-synthase inhibition prolongs survival in murine lupus nephritis.
Systemic lupus erythematosus (SLE) is an autoimmune disease, characterized by nephritis, in which mortality is largely influenced by the severity of renal involvement. As there are evidences that thromboxane (TX)A2 plays an important role in the pathogenesis of lupus nephritis, we decided to assess the effects of long-term suppression of TXA2 synthesis on the progression of the disease, by designing a study of TXA2-synthase inhibition having adequate size to detect an effect on mortality as the primary end-point. Thus, we randomized 362 NZBxNZW mice (11-week-old at entry) to one of the following treatments: a TXA2 synthase inhibitor, FCE 22178 (300 mg/kg daily), saline or cyclophosphamide (5 mg/mouse weekly x 4 weeks) used as reference treatment. The TXA2 synthase inhibitor suppressed TXA2 biosynthesis, as reflected by urinary TXB2 and 2,3-dinor-TXB2 excretion (by 78% and 90%, respectively) and significantly reduced mortality (death rate: 34% vs. 61% in controls, at 37 weeks, P < 0.01). A significant reduction in proteinuria (9 +/- 1.6 vs. 17.3 +/- 2.4 mg/24 hr in FCE 22178 vs. saline, P < 0.01) and glomerular lesions was observed up to 30 weeks but not at 37 weeks. In contrast, cyclophosphamide prevented the development of proteinuria and histologic lesions, and reduced mortality to 8% at 37 weeks. Renal plasma flow and glomerular filtration rate were lower (by 29% and 52%, respectively) in 37-week-old as compared to young NZBxNZW mice. These parameters were further depressed by cyclophosphamide (by 48% and 45% vs. age-matched controls, respectively, P < 0.01) but were not altered significantly by FCE 22178.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Abnormalities of endocrine function in patients with clinically "silent" adrenal masses.
Because, in recent years, patients with incidentally discovered adrenal masses have been encountered increasingly, their endocrine function was investigated in basal conditions and after dynamic tests. Thirty-two patients (23 women and 9 men, aged 28-74 years) were studied. Lesion diameter, as documented by computed tomography and/or nuclear magnetic resonance imaging, ranged between 5 and 65 mm; the tumors were localized on the right in 22 patients, on the left in 5 and bilaterally in 5 cases. In basal conditions, urinary free cortisol (UFC) excretion, plasma adrenocorticotropin (ACTH) and cortisol levels were normal, except for 4 patients who showed high UFC and ACTH levels in the low-normal range. Ovine corticotropin-releasing hormone (CRH, 1 microgram/kg iv) was given to 18 patients, inducing normal ACTH and cortisol responses in 12, blunted responses in 4 and no response in 2 cases. No reduction in ACTH and cortisol levels after suppression tests was observed in 4 of 29 patients after dexamethasone (1 mg overnight) or in 6 of 29 after loperamide. The 4 patients who were unresponsive to both tests did not show any further inhibition after high-dose dexamethasone administration, had low plasma ACTH levels and showed impaired or absent responses to the CRH test: they were diagnosed as affected with preclinical Cushing's syndrome. An exogenous ACTH test performed in 30 patients caused a normal cortisol rise. Basal mean 17-hydroxy-progesterone (17-OHP) levels were not different from those in normal subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
17-alpha-Hydroxyprogesterone↗
Agents combining thromboxane receptor antagonism with thromboxane synthase inhibition: [[[2-(1H-imidazol-1-yl)ethylidene]amino]oxy]alkanoic acids.
A new class of compounds combining thromboxane-A2 (TxA2) receptor antagonism and thromboxane synthase inhibition is described. A first series of (E)- and (Z)-[[[2-(1H-imidazol-1-yl)ethylidene]amino]oxy]pentanoic acids showed relevant thromboxane synthase inhibition associated with weak TxA2 receptor antagonism, while a series of (+/-)-(E)-[[[2-(1H-imidazol-1-yl)-3-phenylpropylidene]amino]oxy] pentanoic acids, structurally derived from the former, showed potent and well-balanced dual activity. Structural requirements for significant single and dual activity are discussed. Two close congeners of the latter series, (+/-)-(E)-5-[[[1-cyclohexyl-2-(1H-imidazol-1-yl)-3- phenylpropylidene]amino]oxy]pentanoic acid 23c and its p-fluorophenyl analog 23m, inhibited TxB2 production in vitro, in rat whole blood during clotting, with IC50 of 0.06 and 0.37 microM and antagonized the binding of [3H]SQ 29548 to washed human platelets, with IC50 of 0.08 and 0.02 microM, respectively. These two compounds were selected for further pharmacological evaluation and were shown to antagonize U46619-induced platelet aggregation in human platelet rich plasma with IC50 of 0.30 and 0.44 microM, respectively. They were both orally available, and in particular 23m caused a long lasting ex vivo TxA2 synthase inhibition in the fed rat. The levorotatory enantiomer of 23c, stereospecifically synthesized as a model compound, was found to be more potent than racemic 23c with regard to TxA2 receptor antagonism (IC50 = 0.04 microM) and equivalent to the latter with regard to TxA2 synthase inhibition. A molecular modeling study concerning the levorotatory enantiomer of 23c (S), TxA2, and representative TxA2 antagonists of different classes led to the definition of a putative pharmacophoric model for the TxA2 receptor ligands.
15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
Consequences of acute nitric oxide synthesis inhibition in experimental glomerulonephritis.
To assess the functional relevance of the enhanced glomerular nitric oxide (NO) synthesis during acute nephrotoxic serum (NTS) nephritis, a NO synthesis inhibitor (NOI) NG-monomethyl-L-arginine was administered to normal (N + NOI) and acutely nephritic (NTS + NOI) Munich-Wistar rats, and systemic and glomerular hemodynamic responses were contrasted with those observed in vehicle-treated normal and nephritic (NTS) controls. Urinary protein excretion rates were equal in normal and N + NOI rats but were markedly elevated in NTS animals and further increased in NTS+NOI. NO inhibition in normal animals (normal versus N + NOI) led to reductions in glomerular plasma flow rate and the glomerular capillary ultrafiltration coefficient (Kf) and elevations in afferent and efferent arteriolar resistances and net transcapillary hydraulic pressure difference (delta P), as well as an increase in systemic arterial pressure. The increase in delta P offset the falls in glomerular plasma flow rate and Kf, and GFR was preserved. Directionally similar responses in efferent resistance occurred in NTS + NOI compared with NTS, however, afferent resistance was not further affected by NOI. Additionally, although Kf was severely depressed in the NTS group (approximately 60% versus normal), it was not further depressed by NOI treatment. Polymorphonuclear cell (PMN) infiltration/glomerulus was mildly increased in N + NOI over normal. In contrast, PMN number in NTS + NOI rats was diminished as compared with NTS.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Value of serum dehydroepiandrosterone sulfate assay in the evaluation of pituitary-adrenal insufficiency after pituitary adenomectomy.
The value of dehydroepiandrosterone sulfate (DHEA-S), a specific marker of adrenal androgen production, in the assessment of clinical states of hypercortisolism and hypocortisolism has been suggested. Since the way to simply test for ACTH reserve in patients (pts) with pituitary tumors after adenomectomy is not standardized, in this study serum DHEA-S concentration was measured in order to establish whether its determination might be a sensitive index of ACTH deficiency. Serum DHEA-S concentration was evaluated in 29 pts with hypothalamic-pituitary tumors (16 females, 13 males, aged 20-70 yr), 14 of whom had GH-secreting adenomas, 13 nonfunctioning adenomas, 1 prolactinoma and 1 craniopharyngioma. Serum DHEA-S and cortisol (F) levels were determined both before and every day for 8 days after pituitary adenomectomy. Before surgery in all pts mean DHEA-S and F basal values were 3.57 +/- 0.42 mumol/L and 391.8 +/- 29.0 nmol/L, respectively. Eight out of 29 pts showed reduced DHEA-S levels (0.85 +/- 0.19 mumol/L), which remained lower than normal in the postsurgical period; on the contrary, F levels were reduced in only 2 and 3 cases before and after surgery, respectively. In 3 other pts DHEA-S levels were normal before surgery and then were low in the postoperative period, while serum cortisol remained normal in all cases. In most of these patients, the finding of impaired responses to hypothalamic-pituitary-adrenal tests, together with a reduced corticosteroid urinary excretion, confirmed the existence of a secondary hypoadrenalism and the necessity for an adequate replacement therapy.(ABSTRACT TRUNCATED AT 250 WORDS)
Adenoma↗
Effects of racemic, S- and R-indobufen on cyclooxygenase and lipoxygenase activities in human whole blood.
Racemic indobufen inhibits human platelet aggregation by reducing thromboxane (TX) A2 biosynthesis. In order to ascertain which of the two optical isomers is responsible for its pharmacological activity, we compared the effects of racemic (SR +/-), S(+) enantiomer and R(-) enantiomer indobufen on cyclooxygenase and 5-lipoxygenase activities by assessing the biosynthesis of TXB2, prostaglandin (PG) E2 and leukotriene (LT) B4 in human whole blood stimulated with the Ca2+ ionophore A23187. Racemic indobufen caused a dose-dependent inhibition of TXB2 and PGE2 production (IC50: 0.53 +/- 0.06 and 0.34 +/- 0.02 micrograms/ml, respectively; mean +/- S.D., n = 4). S-Indobufen was approximately 2-fold more potent than the racemate in inhibiting the synthesis of cyclooxygenase products. R-Indobufen affected the same enzyme but only at considerably higher concentrations (IC50: 53 +/- 8 micrograms/ml, n = 3). Serum LTB4 concentrations were significantly reduced only at indobufen concentrations greater than 50 micrograms/ml. In conclusion, indobufen is a selective inhibitor of the cyclooxygenase activity of platelet PGG/H synthase in a concentration range corresponding to the therapeutic plasma levels in man. This inhibitory effect is largely due to the S isomer of the drug.
Adult↗
Screening tests for Cushing's syndrome.
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Adolescent↗
Precocious puberty in a boy with a PRL-, LH- and FSH-secreting pituitary tumour: hormonal and immunocytochemical studies.
The case of a 7-year-old boy affected with precocious puberty and a large intra- and suprasellar pituitary tumour is described. He had hyperprolactinemia and elevated serum LH, FSH and testosterone concentrations. Pre-operative dynamic hormonal studies showed a rise of PRL, LH and FSH levels after TRH (200 micrograms iv) and a rise of LH and FSH after GnRH (100 micrograms iv). Dopamine infusion (4 micrograms.kg-1.min-1 for 180 min) did not affect gonadotropins and greatly reduced serum PRL. GnRH analogue (buserelin, 0.5 mg sc t.i.d. for 10 days) administration inhibited both LH and FSH, but did not affect PRL concentration. Serum LH and FSH increased after ethinyl-estradiol (0.5 mg orally) administration, and were not affected by bromocriptine (5-7.5 mg/day for 10 days), which decreased serum PRL levels. The patient underwent transfrontal neurosurgery and a large tumour mass was completely removed. Morphological study of the excised tumour, by electron microscope double label immunotechnique, revealed that a large number of tumour cells (70-85%) were positive for PRL, LH and FSH, co-localized in the same secretory granule. After neurosurgery, serum PRL, LH, FSH and testosterone levels fell to within the normal limits. Two months later the patient was well and signs of precocious puberty had partially regressed; hormone levels were in the normal range and MR imaging control did not demonstrate any residual lesion in the sellar region.
Adenoma↗
Effects of the opiate agonist loperamide on pituitary-adrenal function in patients with suspected hypercortisolism.
In the present work the possible use of loperamide, an opiate agonist, in the dynamic evaluation of patients with suspected hypercortisolism was investigated. The effects of loperamide on plasma ACTH and cortisol levels were evaluated in normal subjects and in 58 patients with suspected Cushing's syndrome. The results were compared to those obtained after the overnight dexamethasone suppression test. In normal subjects plasma ACTH and cortisol levels were significantly (p less than 0.005) suppressed by both loperamide (16 mg po) and dexamethasone (1 mg po). In 17 patients, in whom the diagnosis of Cushing's syndrome was confirmed by subsequent investigations, neither loperamide or dexamethasone inhibited cortisol (from a baseline of 606 +/- 55 nmol/L) to a nadir of 502 +/- 43 nmol/L and 539 +/- 50 nmol/L, respectively) and ACTH concentration (from a basal level of 70.1 +/- 11.8 pg/ml to a nadir of 46.0 +/- 8.6 pg/ml and 54.3 +/- 7.5 pg/ml, respectively). In 34 patients, in whom the suspect of hypercortisolism was ruled out, either loperamide or dexamethasone suppressed the pituitary-adrenal axis: cortisol and ACTH levels significantly fell from 417 +/- 24 nmol/L and 28.3 +/- 3.5 pg/ml to 60 +/- 6 nmol/L and 14.4 +/- 1.4 pg/ml after loperamide and to 26 +/- 4 nmol and 16.4 +/- 1.7 pg/ml after dexamethasone. In 7 patients discordant responses were observed. In 3 patients treated with antiepileptic drugs ACTH and cortisol levels were inhibited by loperamide, but not by dexamethasone.(ABSTRACT TRUNCATED AT 250 WORDS)
Adrenocortical Hyperfunction↗
Addison's disease and empty sella.
A 47-year-old woman affected by Addison's disease, inadequately treated with corticosteroids for 14 yr, was referred to our clinic. As a x-ray of skull revealed an enlarged sella turcica, a more thorough study of hypothalamic-pituitary function and of the sellar region was performed. The normal suppression of high plasma ACTH levels induced by hydrocortisone infusion and the normal pattern of ACTH, TSH, PRL, LH and FSH to appropriate stimuli (CRH, TRH, GnRH) excluded the possible existence of an ACTH-secreting adenoma; the CT scan images showed the presence of an empty sella. The impaired GH rise after GHRH may be attributed to either the empty sella or the adrenal failure. This is the first patient with Addison's disease and empty sella, in whom the hypothalamic-pituitary function has been studied by the administration of four releasing hormones.
Addison Disease↗
Loperamide modifies but does not block the corticotropin-releasing hormone-induced ACTH response in patients with Addison's disease.
The effect of loperamide - a peripheral opiate agonist - on plasma ACTH response to Corticotropin-releasing Hormone (CRH) has been investigated in 6 patients with Addison's disease. After placebo administration CRH induced a marked ACTH increase. After loperamide administration ACTH levels fell to a nadir of 135 +/- 76 pg/ml, and then CRH was still able to induce an ACTH increase; the pattern of ACTH response to CRH was slightly delayed. There was a significant difference between the two ACTH curves after CRH only in the early phase of the response. These data suggest that the inhibitory role of loperamide on ACTH secretion is exerted at supra-pituitary level, although a pituitary site of action can not be excluded.
Addison Disease↗
[Psychological and social support for patients with mastectomies].
Cancer patients need general emotional support but doctors and nurses often fail to recognise patients needs. This literature review aims at demonstrating the effect of social and psychosocial support on breast cancer women. All the article published from 1980 were reviewed. Psychotherapeutic counselling and psychosocial interventions were given by a range of people, including nurses, psychologists, psychiatrists and volunteers. Unfortunately the poor quality of the studies, which are often small and poorly controlled, does not allow to make a definitive statement on the impact of psychosocial interventions. The multiplicity of types of intervention and outcomes used make comparisons between studies difficult. However, when considered in conjunction with the evidence that informal social support from partners, friends and relatives is associated with better outcomes, this research highlights the importance of psychosocial factors for breast cancer patients.
Counseling↗